Nie Xiaohu, Su Zhongzhou, Yan Renfu, Yan Ai, Qiu Sheng, Zhou Yue
Department of Neurosurgery, Huzhou Central Hospital, Wuxing District, Huzhou, Zhejiang 313000, P.R. China,
Onco Targets Ther. 2018 Dec 21;12:41-49. doi: 10.2147/OTT.S186701. eCollection 2019.
MicroRNA-562 (miR-562) has been found to possess anti-cancer function in certain tumors. However, the function of miR-562 in glioblastoma (GBM) is still not fully understood.
The aim at present study is to analyze the function of miR-562 and its possible target in GBM cells.
In the present study, a total of 80 GBM samples and 16 adjacent noncancerous tissues were used to examine the expression of miR-562 and c-MET. In order to gain a deep insight into the molecular network of miR-562 and c-MET in GBM, the miR-562 mimic and inhibitor were transfected into two GBM cell lines (U251 and U87), respectively. Meanwhile, lentiviral vector was used to mediate overexpression of c-MET. Cell proliferation was examined via Cell Counting Kit-8 (CCK-8) assays. Meanwhile, cell apoptosis was analyzed by Annexin V-FTTC/PI staining assay.
Our results indicated that the level of miR-562 was downregulated in GBM tissues and the expression of c-MET was upregulated in tumors. Cell proliferation analysis indicated that miR-562 was an anti-proliferation effector in GBM cells. Moreover, cell apoptosis analysis suggested the pro-apoptosis function of miR-562 in GBM cells.
Our results demonstrated that miR-562 negatively regulated the c-MET/AKT signal pathway. In addition, caspase-3 might also serve as another target for miR-562 in GBM cells. This research not only obtained a deep understanding of miR-562 but also provided evidence in terms of developing new prognostic biomarker for GBM.
微小RNA-562（miR-562）已被发现在某些肿瘤中具有抗癌功能。然而，miR-562在胶质母细胞瘤（GBM）中的功能仍未完全明确。
本研究旨在分析miR-562在GBM细胞中的功能及其可能的靶标。
在本研究中，共使用80例GBM样本和16例相邻的非癌组织来检测miR-562和c-MET的表达。为深入了解GBM中miR-562和c-MET的分子网络，分别将miR-562模拟物和抑制剂转染到两种GBM细胞系（U251和U87）中。同时，使用慢病毒载体介导c-MET的过表达。通过细胞计数试剂盒-8（CCK-8）检测细胞增殖。同时，通过膜联蛋白V-FTTC/PI染色检测分析细胞凋亡。
我们的结果表明，GBM组织中miR-562水平下调，肿瘤中c-MET表达上调。细胞增殖分析表明，miR-562是GBM细胞中的抗增殖效应因子。此外，细胞凋亡分析提示miR-562在GBM细胞中具有促凋亡功能。
我们的结果表明，miR-562负调控c-MET/AKT信号通路。此外，半胱天冬酶-３也可能是GBM细胞中miR-562的另一个靶标。本研究不仅深入了解了miR-562，还为开发GBM新的预后生物标志物提供了证据。
